Detecting And Treating Patients With Diabetic Autonomic Neuropathy

By Damieon Brown, DPM and Javier La Fontaine, DPM

Autonomic neuropathy may significantly affect the quality of life of patients with diabetes. Unfortunately, despite the common prevalence of this condition in this population, autonomic neuropathy is one of the least understood and recognized complications of diabetes. Not only is there a cloudy picture in regard to the pathogenesis of the condition, there are various clinical manifestations with no degree of consistency in which they may occur. With this in mind, let’s take a closer look at this potentially serious complication among people with diabetes. Autonomic neuropathy generally involves the entire autonomic nervous system and is marked by dysfunction of one or more organ systems. One may notice clinical manifestations of autonomic neuropathy among patients with longstanding diabetes and in those with less acute dysfunction that occurs within one to two years of being diagnosed with diabetes. The pathogenesis of autonomic neuropathy includes theories of metabolic insult to the nerve fibers, neurovascular insufficiency, autoimmune damage and neurohormonal growth factor deficiency. The direct neuronal damage is the result of increased glycemic activation leading to sorbitol accumulation. Some researchers also believe the activation of protein kinase C may be the contributing cause of vasoconstriction and reduction in neuronal blood flow. The combination of increased oxidative stress and increased free radical production may also cause vascular endothelial damage and reduce the bioavailability of nitric oxide.1 A Closer Look At Clinical Manifestations Clinical manifestations of autonomic neuropathy tend to occur simultaneously but not consistently in the same pattern. These patients tend to have cardiovascular, gastrointestinal, gastrourinary, metabolic, sudomotor and pupillary problems.1 Cardiovascular autonomic neuropathy (CAN) has been one of the commonly overlooked complications among patients with diabetes.2 This tends to result from damage to the autonomic nerve fibers that innervate the heart and blood vessels, and cause abnormalities in heart rate and vascular dynamics. CAN may be marked by clinical manifestations such as exercise intolerance, orthostatic hypotension and silent myocardial ischemia. Exercise intolerance in regard to autonomic dysfunction has been shown to have marked effects on decreased heart rate and blood pressure in those with CAN. Orthostatic hypotension usually occurs in the diabetic population due to damage of the efferent sympathetic fibers that are part of the splanchnic vasculature. If patients with diabetes start to complain of symptoms such as lightheadedness, dizziness, fatigue, weakness, blurry vision and neck pain, proceed with further workup in order to differentiate CAN from any other cause associated with these symptoms. Myocardial ischemia is an entity that is not clearly understood. Previous studies suggest that this is caused by damage to the myocardial sensory afferent fibers in the autonomic nerve. If these patients experience chest pain in any location along with confusion, unexplained fatigue, edema, nausea, hemoptysis and vomiting, one should have a high index of suspicion for a silent heart attack. How Does This Relate To The Diabetic Foot? The autonomic nervous system controls microvascular skin flow.3 In the diabetic population, the rhythmic contraction of small vessels such as arterioles, venules and small arteries is affected. Loss of control of these vessels will increase blood flow in the absence of large vessel peripheral arterial occlusive disease. This is also a consequence of increased arteriovenous shunting and results in a warm foot with distended dorsal foot veins.4 According to Low, et. al., this physiological problem may lead to diabetic neuropathy as well.5 This problem resembles premature aging. The clinical pedal manifestations of autonomic neuropathy are dry skin, loss of sweating, distended veins and fissuring, which may lead to ulcerations, infection and gangrene.6 It has been documented in the literature that autonomic neuropathy may increase osteoclastic activity, resulting in reduced bone density. Young, et. al., found reduced bone density in the lower limbs of 17 patients with Charcot in comparison to 10 neuropathic control subjects.7 Therefore, Charcot arthropathy may reflect the severity of autonomic neuropathy.

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